Mechanisms of hypertension in patients with chronic obstructive pulmonary disease and acute respiratory failure

Citation
F. Fontana et al., Mechanisms of hypertension in patients with chronic obstructive pulmonary disease and acute respiratory failure, AM J MED, 109(8), 2000, pp. 621-627
Citations number
40
Categorie Soggetti
General & Internal Medicine","Medical Research General Topics
Journal title
AMERICAN JOURNAL OF MEDICINE
ISSN journal
00029343 → ACNP
Volume
109
Issue
8
Year of publication
2000
Pages
621 - 627
Database
ISI
SICI code
0002-9343(200012)109:8<621:MOHIPW>2.0.ZU;2-2
Abstract
PURPOSE: To investigate the effects of hypoxemia, hypercapnia, and cardiova scular hormones (norepinephrine, endothelin-l, and atrial natriuretic facto r) on blood pressure during acute respiratory failure. PATIENTS AND METHODS: Patients with chronic obstructive pulmonary disease a nd acute respiratory failure were divided into four groups of 10 patients e ach: hypoxemia-normocapnia, hypoxemia-hypercapnia, hypoxemia-hypocapnia, an d normoxemia-hypercapnia. Plasma norepinephrine levels were determined by h igh-performance liquid chromatography with electrochemical detection. plasm a endothelin-l and atrial natriuretic factor levels were radioimmunoassayed after chromatographic preextraction. RESULTS: Systolic blood pressure and cardiovascular hormone levels were gre ater in patients with hypercapnia (whether or not they also had hypoxemia) than in those with normocapnia and hypoxemia. For example, in patients with hypercapnia and normoxemia, the mean (+/- SD) systolic blood pressure was 183 +/- 31 mm Hg and the mean norepinephrine level was 494 +/- 107 pg/mL, a s compared with 150 +/- 6 mm Hg and 243 +/- 58 pg/mL in those with normocap nia and hypoxemia (both P <0.05). Similar results were seen for endothelin- 1 and atrial natriuretic factor levels, and for the comparisons of hypoxemi c patients who were hypercapnic with those who were normocapnic. CONCLUSIONS: These results suggest that blood carbon dioxide levels, rather than oxygen levels, are responsible for hypertension during acute respirat ory failure, perhaps as a result of enhanced sympatho-adrenergic activity. (C) 2000 by Excerpta Medics, Inc.